Cortical Mechanisms of Auditory-Vocal Interaction

听觉-声音相互作用的皮质机制

• 批准号: 8960346
• 负责人: STEVEN J ELIADES
• 金额: $ 23.48万
• 依托单位: UNIVERSITY OF PENNSYLVANIA
• 依托单位国家: 美国
• 财政年份: 2014
• 资助国家: 美国
• 起止时间: 2014-12-01 至 2019-11-30
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/8960346
• 关键词: Accelerometer; Acoustics; Address; Animal Experiments; Animal Vocalization; Animals; Area; Auditory; Auditory area; Brain; Brain region; Callithrix; Communication; Detection; Electric Stimulation; Epilepsy; Exhibits; Feedback; Financial compensation; Frequencies; Future; Goals; Health; Hearing; Human; Intractable Epilepsy; Lead; Learning; Measurement; Measures; Methods; Modeling; Monitor; Monkeys; Motor; Motor Cortex; Neural Pathways; Neurons; Operative Surgical Procedures; Patients; Play; Primates; Process; Production; Research; Role; Sensory; Signal Transduction; Site; Source; Speech; Speech Disorders; Testing; Translating; Translations; Voice; Work; frontal lobe; hearing impairment; human subject; motor control; neuromechanism; neurophysiology; neurotransmission; nonhuman primate; novel strategies; relating to nervous system; research study; response; sound; time use; vocal control; vocalization

DESCRIPTION (provided by applicant): The overall objective of this research is to understand how we listen to the sound of our own voice while talking and how we use this information to help control our speech. Humans have sophisticated mechanisms for self-monitoring of this vocal feedback during speech that allow for the detection and compensation for vocal errors. Degradation of this self-monitoring, such as following hearing loss, results in difficulty in acquiring and maintaining normal speech and impairs vocal communication. Recent work in both humans and primates has demonstrated a suppression of neural activity in the auditory cortex during vocalization that may play a role in self-monitoring. The origin and significance of this neural activity is unknown. This proposal focuses on determining the neural mechanism of self-monitoring during vocal production and its role in feedback vocal control, using both human subjects and a vocal primate model, the marmoset monkey. Aim 1 tests the hypothesis that suppressed neurons of the auditory cortex in marmosets exhibit self- monitoring activity, and that this neural activity can drive compensatory vocal control. Auditory cortex neurons are recorded from vocalizing marmosets while altering the frequency content of their vocal feedback to induce vocal compensation. Neural recording is followed by electrical stimulation of the auditory cortex in order to disrupt self-monitoring and resulting feedback compensation. These experiments will demonstrate how vocalization self-monitoring activity in the auditory cortex drives feedback vocal control. Aim 2 tests the hypothesis that frontal cortical areas, particularl pre-motor cortex, are the origin of the neural signals that cause vocal suppression in auditory cortex. Neurons in both frontal and auditory cortex of marmosets are recorded simultaneously and quantitative analyses applied to demonstrate neural connectivity between brain regions during vocal production. These results will demonstrate the neural pathways beyond auditory cortex that contribute to vocal self-monitoring. Aim 3 tests the hypothesis that human auditory cortex is necessary for self-monitoring and feedback vocal control of speech. Auditory cortex activity is recorded using intracranial electrocorticographic activity in patients undergoing neura monitoring for epilepsy surgery. Paralleling the animal experiments, electrical stimulation of cortex is performed during pitch-altered speech feedback to demonstrate the role of auditory cortex in feedback compensation. These experiments will have implications for understanding speech motor control and will allow mechanistic comparisons between human speech and animal vocalization. Such comparisons are critical as we attempt to translate results from animal neurophysiology towards understanding human speech production.

描述（由申请人提供）：这项研究的总体目标是了解我们在说话时如何倾听自己的声音，以及我们如何利用这些信息来帮助控制我们的语言。人类有复杂的机制来自我监控说话过程中的声音反馈，从而发现和补偿声音错误。这种自我监控的退化，如听力丧失，会导致难以获得和维持正常的语言，并损害声音交流。最近对人类和灵长类动物的研究表明，在发声过程中，听觉皮层的神经活动受到抑制，这可能在自我监控中发挥作用。这种神经活动的起源和意义尚不清楚。本研究的重点是确定声音产生过程中自我监控的神经机制及其在反馈声音控制中的作用，研究对象包括人类受试者和一种发声灵长类动物模型——狨猴。目的1验证了狨猴听觉皮层中被抑制的神经元表现出自我监控活动的假设，并且这种神经活动可以驱动代偿性声音控制。在改变狨猴声音反馈的频率内容以诱导声音补偿的同时，记录了狨猴发声的听觉皮层神经元。神经记录之后是对听觉皮层的电刺激，以破坏自我监控和由此产生的反馈补偿。这些实验将证明听觉皮层中的发声自我监控活动如何驱动反馈发声控制。目的2验证了额叶皮质区域，特别是前运动皮质，是引起听觉皮层声音抑制的神经信号的来源的假设。同时记录了狨猴额叶皮层和听觉皮层的神经元，并应用定量分析来证明在发声过程中大脑区域之间的神经连接。这些结果将证明听觉皮层以外的神经通路有助于声音自我监控。目的3验证了人类听觉皮层是语音自我监控和反馈语音控制所必需的假设。在接受癫痫手术神经监测的患者中，使用颅内皮质电图活动记录听觉皮层活动。在动物实验的基础上，在变音高语音反馈过程中对皮层进行电刺激，以证明听觉皮层在反馈补偿中的作用。这些实验将对理解语言运动控制产生影响，并将允许在人类语言和动物发声之间进行机制比较。当我们试图将动物神经生理学的结果转化为理解人类语言产生时，这种比较是至关重要的。